• Metabolic alkalosis is defined as increased serum bicarb (HCO3-) concentration.
• Metabolic alkalosis is caused by either:
Increased renal excretion of H+ ions/ reabsorption of HCO3- ions in hyperaldosteronis or renal tubular disorders
GI H+/Cl- loss in vomiting, laxative abuse, villous adenoma, or congenital chloride diarrhea
GI HCO3- gain due to ingestion of sodium bicarb tabs or antacid plus kayexalate
IV infusion of sodium bicarb or sodium citrate in large volume blood tranfusion or fresh frozen plasma in plasmapheresis
Intracellular H+ shift in severe hypokalemia
Skin Cl- loss due to excessive sweating in cystic fibrosis
• Metabolic aklalosis is further categorized into chloride-responsive and chloride-unresponsive
Chloride-responsive (or chloride-sensitive): associated with NaCl deficiency and extracellular volume (ECV) depletion (hence can be corrected with NaCl infusion)
Chloride-unresponsive (or chloride-resistant): associated with mineralocorticoid excess/ hyperactivity causing NaCl retention and ECV expansion and cannot be corrected with NaCl infusion
• Additional diagnostic tests used to identify causes of metabolic alkalosis include:
Urine chloride: differentiates between Cl-responsive vs Cl-unresponsive metabolic alkalosis
Serum renin and aldosterone: used to differentiate between 1° vs 2° hyperaldosteronism vs other conditions causing mineralocorticoid hyperactivity
